This content is about Autoimmune Nervous System Disorders. This content is fruitful for BScN.-III Year & GNM II Year Students.

1. UNIT-3
NEUROLOGICAL DISORDERS
BY- AHMED SODHA
M.Sc.(N)- M.S.N.

2. AUTOIMMUNE
NERVOUS SYSTEM
DISORDERS
 THIS INCLUDE:
 THIS INCLUDE:
i. MULTIPLE SCLEROSIS,
ii. MYASTHENIA GRAVIS, AND
iii. GUILLAIN-BARRÉ SYNDROME.

5. DEFINITION:- “MULTIPLE SCLEROSIS (MS) IS AN
IMMUNE-MEDIATED PROGRESSIVE DEMYELINATING
DISEASE OF THE CNS. IT RESULTS IN IMPAIRED
TRANSMISSION OF NERVE IMPULSES”.
 DEMYELINATION REFERS TO THE DESTRUCTION OF
MYELIN. (MYELIN - THE FATTY AND PROTEIN
MATERIAL THAT SURROUNDS CERTAIN NERVE FIBERS
IN THE BRAIN AND SPINAL CORD).
IN THE BRAIN AND SPINAL CORD).
 INCIDENCE - MS TYPICALLY PRESENTS IN YOUNG
ADULTS AGES 20 TO 40, AND IT AFFECTS WOMEN
MORE FREQUENTLY THAN MEN.

6.  IN MS, THE IMMUNE SYSTEM ATTACKS THE
PROTECTIVE SHEATH (MYELIN) THAT COVERS NERVE
FIBERS AND CAUSES COMMUNICATION PROBLEMS
BETWEEN YOUR BRAIN AND THE REST OF YOUR
BODY.
 THE DISEASE CAN CAUSE PERMANENT DAMAGE OR
DETERIORATION OF THE NERVES.
 THERE'S NO CURE FOR MULTIPLE SCLEROSIS.
 HOWEVER, TREATMENTS CAN HELP SPEED
RECOVERY FROM ATTACKS, MODIFY THE COURSE OF
THE DISEASE AND MANAGE SYMPTOMS.

7. ETIOLOGY:-
• IDIOPATHIC
• AUTOIMMUNITY
• GENETICAL FACTOR
• AGING
 NORMAL PHYSIOLOGY:
 SENSITIZED ‘T-CELLS’ TYPICALLY CROSS THE
BLOOD BRAIN BARRIER; THEIR FUNCTION IS TO
CHECK THE CNS FOR ANTIGENS AND THEN LEAVE.

8. P.P.:- DUE TO ETIOLOGY
SENSITIZED T CELLS REMAIN IN THE CNS
THAT ATTACK MYELIN
ATTACK LEADS TO INFLAMMATION ON MYELIN &
THAT DESTROYS MYELIN
DEMYELINATED AXONS
FURTHER INTERRUPTING THE TRANSMISSION OF
IMPULSES

9. C.M.:-
 SIGNS AND SYMPTOMS OF MS VARY WIDELY AND
DEPEND ON THE AMOUNT OF NERVE DAMAGE AND
WHICH NERVES ARE AFFECTED.
 MULTIPLE SCLEROSIS SIGNS AND SYMPTOMS MAY
DIFFER GREATLY FROM PERSON TO PERSON AND
OVER THE COURSE OF THE DISEASE DEPENDING ON
OVER THE COURSE OF THE DISEASE DEPENDING ON
THE LOCATION OF AFFECTED NERVE FIBERS.
 THE AREAS MOST FREQUENTLY AFFECTED ARE THE
OPTIC NERVES, OPTIC CHIASM, THE CEREBRUM; THE
BRAIN STEM AND CEREBELLUM; AND THE SPINAL
CORD.

10. C.M.:-
•FATIGUE
• NUMBNESS OR WEAKNESS IN ONE OR MORE LIMBS
THAT TYPICALLY OCCURS ON ONE SIDE OF YOUR
BODY AT A TIME, OR THE LEGS AND TRUNK
• DIFFICULTY IN COORDINATION
• LOSS OF BALANCE
• PAIN
• PAIN
• BLURRING VISION
• DIPLOPIA (PROLONGED DOUBLE VISION)
• TINGLING IN PARTS OF BODY
• PROBLEMS WITH SEXUAL, BOWEL AND BLADDER
FUNCTION

11. D.E.:- THERE ARE NO SPECIFIC TESTS FOR MS
• H.C. & P.E.
• NEUROLOGICAL EXAMINATION
• CT SCAN
• MRI

12. TREATMENT:- THERE IS NO CURE FOR MULTIPLE
SCLEROSIS. TREATMENT TYPICALLY FOCUSES ON
THE PROGRESSION OF THE DISEASE AND
MANAGING MS SYMPTOMS
 MEDICATION
 CORTICOSTEROIDS (ORAL PREDNISONE, AND
I.V. METHYLPREDNISONE TO REDUCE NREVE
INFLAMMATION)
 INTERFERONS (BETA-1A, BETA-1B)
 GLATIRAMER ACETATE (IMMUNOMODULATOR
 GLATIRAMER ACETATE (IMMUNOMODULATOR
AGENT ) (COPAXONE, GLATOPA)
[ THIS MEDICATION MAY HELP BLOCK YOUR IMMUNE
SYSTEM'S ATTACK ON MYELIN AND MUST BE INJECTED
BENEATH THE SKIN. SIDE EFFECTS MAY INCLUDE SKIN
IRRITATION AT THE INJECTION SITE.]
 MITOXANTRONE (ANTI-NEOPLASTIC AGENT)
 PHYSICAL THERAPY
 PLASMAPHERESIS

13.  INTERFERONS:- ARE A FAMILY OF NATURALLY-
OCCURRING PROTEINS THAT ARE MADE AND
SECRETED BY CELLS OF THE IMMUNE SYSTEM (FOR
EXAMPLE, WHITE BLOOD CELLS, NATURAL KILLER
CELLS, FIBROBLASTS, AND EPITHELIAL CELLS).
THREE CLASSES OF INTERFERONS HAVE BEEN
IDENTIFIED:
• ALPHA,
• BETA, AND
BETA, AND
• GAMMA.
 PLASMAPHERESIS THE LIQUID PORTION OF PART
OF YOUR BLOOD (PLASMA) IS REMOVED AND
SEPARATED FROM YOUR BLOOD CELLS. THE BLOOD
CELLS ARE THEN MIXED WITH A PROTEIN SOLUTION
(ALBUMIN) AND PUT BACK INTO YOUR BODY. PLASMA
EXCHANGE MAY BE USED IF YOUR SYMPTOMS ARE
NEW, SEVERE AND HAVEN'T RESPONDED TO
STEROIDS

15. DEFINITION:-
“MYASTHENIA GRAVIS, AN AUTOIMMUNE DISORDER
AFFECTING THE MYONEURAL JUNCTION, IS
CHARACTERIZED BY VARYING DEGREES OF
WEAKNESS OF THE VOLUNTARY MUSCLES”.
 IT'S CAUSED BY A BREAKDOWN IN THE NORMAL
COMMUNICATION BETWEEN NERVES AND MUSCLES.
 THOUGH THIS DISEASE CAN AFFECT PEOPLE OF
ANY AGE, IT'S MORE COMMON IN WOMEN YOUNGER
THAN 40 AND IN MEN OLDER THAN 60.

16.  NORMAL PHYSIOLOGY:
YOUR NERVES COMMUNICATE WITH YOUR MUSCLES
BY RELEASING CHEMICALS (NEUROTRANSMITTERS)
THAT FIT PRECISELY INTO RECEPTOR SITES ON THE
MUSCLE CELLS AT THE NERVE-MUSCULAR JUNCTION
 PATHOLOGY:
 IN MYASTHENIA GRAVIS, YOUR IMMUNE SYSTEM
PRODUCES ANTIBODIES THAT BLOCK OR DESTROY
MANY OF YOUR MUSCLES' RECEPTOR SITES FOR A
MANY OF YOUR MUSCLES' RECEPTOR SITES FOR A
NEUROTRANSMITTER CALLED ACETYLCHOLINE.
 ONLY FEWER RECEPTOR SITES AVAILABLE, YOUR
MUSCLES RECEIVE FEWER NERVE SIGNALS,
RESULTING IN WEAKNESS.
 THYMUS GLAND TRIGGERS OR MAINTAINS THE
PRODUCTION OF THE ANTIBODIES THAT BLOCK
ACETYLCHOLINE.

18.  P.P.:- DUE TO ETIOLOGY
AUTO ANTIBODIES DIRECTED TO MYONEURAL
JUNCTION
DESTROY MUSCLES' RECEPTOR SITES
MUSCLES RECEIVE FEWER NERVE SIGNALS
WEAKNESS OF MUSCLES

19.  ETIOLOGY:-
• IDIOPATHIC
• AUTOIMMUNITY
• TUMOR OF THYMUS GLAND
• GENETICAL FACTOR
• AGING
 C.M.:-
• PTOSIS (DROOPING OF THE EYE LIDS)
• PTOSIS (DROOPING OF THE EYE LIDS)
• DIPLOPIA
• WEAKNESS OF FACE & THROAT MUSCLES SO,
IMPAIR SPEAKING, DYSPHAGIA, CHEWING DIFFICULTY,
• WEAKNESS IN NECK, ARMS & LEGS
• DIFFICULTY IN WALKING, CATCHING THE OBJECTS

20.  D.E.:-
• H.C. & P.E. , BLOOD TEST, CT-SCAN & MRI
• EDROPHONIUM TEST
(EDROPHONIUM CHLORIDE (TENSILON) IS INJECTED INTRAVENOUSLY,
2-10mg. THIRTY SECONDS AFTER INJECTION, FACIAL MUSCLE WEAKNESS
AND PTOSIS SHOULD RESOLVE FOR ABOUT 5 MINUTES. THIS IMMEDIATE
IMPROVEMENT IN MUSCLE STRENGTH AFTER ADMINISTRATION OF THIS
AGENT REPRESENTS A ‘POSITIVE TEST’ AND USUALLY CONFIRMS THE
AGENT REPRESENTS A ‘POSITIVE TEST’ AND USUALLY CONFIRMS THE
DIAGNOSIS.)
• REPETITIVE NERVE STIMULATION TEST
(IN THIS NERVE CONDUCTION STUDY, DOCTORS ATTACH ELECTRODES TO
YOUR SKIN OVER THE MUSCLES TO BE TESTED. DOCTORS SEND SMALL
PULSES OF ELECTRICITY THROUGH THE ELECTRODES TO MEASURE THE
NERVE'S ABILITY TO SEND A SIGNAL TO YOUR MUSCLE.)

21.  TREATMENT:-
• CHOLINESTERASE INHIBITORS
(PYRIDOSTIGMINE AND NEOSTIGMINE)
(IT ENHANCE COMMUNICATION BETWEEN NERVES AND MUSCLES. THESE
MEDICATIONS AREN'T A CURE, BUT THEY CAN IMPROVE MUSCLE
CONTRACTION AND MUSCLE STRENGTH)
• CORTICOSTEROIDS (PREDNISONE)
• IMMUNOSUPPRESSANTS
(AZATHIOPRINE, CYCLOSPORINE)
• PLASMAPHERESIS
 SURGERY:-
• THYMECTOMY

22. GUILLAIN - BARRÉ SYNDROME

24.  DEFINITION:-
GUILLAIN-BARRÉ SYNDROME IS AN AUTOIMMUNE
ATTACK OF THE PERIPHERAL NERVE MYELIN THAT
RESULT IN DEMYELINATION OF PERIPHERAL NERVES
AND CHARACTERIZED BY WEAKNESS, HYPOREFLEXIA,
AND NUMBNESS.
 ETIOLOGY:-
 ETIOLOGY:-
• IDIOPATHIC
• AUTOIMMUNITY
• SECONDARY TO RESPIRATORY & G.I. INFECTION
• GENETICAL FACTOR
• AGING

25.  P.P.:- DUE TO ETIOLOGY
ANTIBODIES REACT TOWARDS MYELIN OF
PERIPHERAL NERVOUS SYSTEM
ANTIBODIES DESTRUCT MYELIN PROTEIN
RESULTS IN DYSKINESIA, HYPOREFLEXIA, AND
PARESTHESIA
RESULTS IN DYSKINESIA, HYPOREFLEXIA, AND
PARESTHESIA
• DYSKINESIA (INABILITY TO EXECUTE VOLUNTARY MOVEMENTS)
• PARESTHESIA (NUMBNESS)

26.  C.M.:-
• BEGINS WITH TINGLING AND WEAKNESS STARTING
IN YOUR FEET AND LEGS AND SPREADING TO YOUR
UPPER BODY AND ARMS “(ASCENDING FEATURE)”
• PRICKLING, PINS AND NEEDLES SENSATIONS IN
YOUR FINGERS, TOES, ANKLES OR WRISTS
• WEAKNESS IN YOUR LEGS THAT SPREADS TO YOUR
UPPER BODY
• UNSTEADY WALKING OR INABILITY TO WALK OR
CLIMB STAIRS

27.  D.E.:-
• GUILLAIN-BARRÉ SYNDROME CAN BE DIFFICULT TO
DIAGNOSE IN ITS EARLIEST STAGES.
• ITS SIGNS AND SYMPTOMS ARE SIMILAR TO THOSE
OF OTHER NEUROLOGICAL DISORDERS AND MAY VARY
FROM PERSON TO PERSON
• H.C. & P.E.
• NEUROLOGICAL EXAMINATION
• LUMBAR PUNCTURE (CSF ANALYSIS)
• LUMBAR PUNCTURE (CSF ANALYSIS)
• ELECTROMYOGRAPHY (THIN-NEEDLE ELECTRODES
ARE INSERTED INTO THE MUSCLES, & THE
ELECTRODES MEASURE NERVE ACTIVITY IN THE
MUSCLES)
• CT-SCAN & MRI

28.  TREATMENT:-
• THERE'S NO CURE FOR GUILLAIN-BARRÉ SYNDROME.
• BUT TWO TYPES OF TREATMENTS CAN SPEED
RECOVERY AND REDUCE THE SEVERITY OF THE
ILLNESS:
i. PLASMAPHERESIS
ii. IMMUNOGLOBULIN THERAPY
(HEALTHY ANTIBODIES IS GIVEN INTRAVENOUSLY)
• PHYSICAL THERAPY
• ACTIVE & PASSIVE EXERCISES